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Case ReportPsychogenic Polydipsia: The Result, or Cause
of,Deteriorating Psychotic Symptoms? A Case Report ofthe
Consequences of Water Intoxication
Melissa Gill1 and MacDara McCauley2
1Cavan/Monaghan Mental Health Services, Drumalee Primary Care
Building, Cootehill Road, County Cavan, Ireland2St. Brigid’s
Hospital, Ardee, County Louth, Ireland
Correspondence should be addressed to Melissa Gill;
[email protected]
Received 4 October 2014; Revised 29 December 2014; Accepted 31
December 2014
Academic Editor: Toshiya Inada
Copyright © 2015 M. Gill and M. McCauley. This is an open access
article distributed under the Creative Commons AttributionLicense,
which permits unrestricted use, distribution, and reproduction in
any medium, provided the original work is properlycited.
Water intoxication is a rare condition characterised by
overconsumption of water. It can occur in athletes engaging in
endurancesports, users of MDMA (ecstasy), and patients receiving
total parenteral nutrition. This case outlines water intoxication
ina patient with psychogenic polydipsia. When the kidney’s capacity
to compensate for exaggerated water intake is exceeded,hypotonic
hyperhydration results. Consequences can involve headaches,
behavioural changes, muscular weakness, twitching,vomiting,
confusion, irritability, drowsiness, and seizures. Cerebral oedema
can lead to brain damage and eventual death. In thiscase,
psychogenic polydipsia led to significant hyponatraemia, cerebral
oedema, and tonic-clonic seizures. Differential diagnosesfor
hyponatraemia are outlined. The aetiology of psychogenic polydipsia
is uncertain, but postulated hypotheses are explored.Psychogenic
polydipsia occurs in up 20% of psychiatric patients and this case
serves to remind us to be cognizant of wateroverconsumption.
1. Introduction
Water intoxication is a rare condition characterised by
over-consumption of water. In the case outlined below, it emergedas
a result of psychogenic polydipsia. Other scenarios caninclude
athletes engaging in endurance sports, users ofMDMA(ecstasy), and
iatrogenic causes, for example, patientsreceiving total parenteral
nutrition. This case describes apatient who, as result of
psychogenic polydipsia, developedserious consequences of
hyponatraemia. With psychogenicpolydipsia occurring in up to 20% of
psychiatric patients, thepotentially fatal consequences cannot be
ignored. Althoughpsychogenic polydipsia has been previously
described inthe literature, this case highlights the fact that a
commonsymptom can be trivialized if not regularly highlighted.
Webelieve that this case report serves as a reminder of animportant
clinical lesson.
2. Case Presentation
A 43-year-old man with a previous diagnosis of bipolardisorder
and alcohol dependence was admitted as an invol-untary patient. He
had been agitated and was irritableprior to admission, engaging in
uncharacteristic behaviorssuch as blowing smoke in his son’s face
and kicking thefamily pet. He admitted to feeling paranoid that
people weretalking about him and described poor sleep, appetite,
energy,and concentration. He appeared perplexed and
thought-disordered and displayed poor insight, repeatedly
expressinga desire to be discharged home. Medications on
admissionincluded nortriptyline 30mg nocte and zopiclone
7.5mgnocte. Risperidone 3mg nocte was commenced.
He had had six admissions to hospital in the three yearssince
his diagnosis and had completed twelve sessions of ECTfor a
prolonged depressive episode just three months prior
Hindawi Publishing CorporationCase Reports in PsychiatryVolume
2015, Article ID 846459, 3
pageshttp://dx.doi.org/10.1155/2015/846459
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2 Case Reports in Psychiatry
to this admission. During the course of his admission,
hisbehaviour deteriorated significantly. He refused to attend
toself-care, exposed his genitals on a number of occasions,
andattempted tomasturbate in front of patients and staff. Becauseof
his unmanageable behaviour, he was briefly secludedon two
occasions. Risperidone was changed to olanzapine,nortriptyline was
discontinued, and sodium valproate wascommenced.
It was noted by staff that the patient was consuming copi-ous
quantities of water on the ward. He was also witnessedto
self-induce vomiting and, on questioning, stated that hewas
drinking excessively in order to induce vomiting. Healso expressed
concerns about frequent micturition. Sodiumlevels were checked and
were found to be 128mmol/L onday 40 of admission. In light of his
escalating abnormalbehaviour, a CT scan was requested and this was
performedon day 53 of admission. An initial verbal report
indicatedthat no abnormalities were detected. On the same day,
hissodium valproate was reduced and subsequently stopped onday 56,
due to lack of response. Clinical notes indicatedthat the patient’s
behaviour continued to deteriorate. Hebecame increasingly
disinhibited in the days after his CTscan, exposing himself to
staff and fellow patients. Thedeterioration in his behaviour
culminated in his urinatingpublicly on the ward and at the
statutory review of hisinvoluntary detention, he reported that God
had instructedhim to do so.
On day 57 of admission, the patient was witnessed bynursing
staff having a tonic-clonic seizure.Thedoctor on dutywas present on
the ward and an ambulance was immediatelycalled. The seizure was
prolonged, failing to respond to twoadministrations of rectal
Diazepam prior to the arrival ofthe ambulance. The patient was
transported to the localgeneral hospital where he underwent a
second CT scan,showing significant cerebral oedema this time. On
admissionhis level of sodium was 108mmol/L. He was treated in
ICUfor 6 days and was discharged home following
psychiatricassessment in the general hospital. His psychiatric care
wastaken over by the local Home Based Treatment Team. He
hasremained seizure-free and is being successfully treated in
thecommunity from a mental health point of view. He was notoffered
general medical follow-up.
3. Discussion
Hyponatraemia is defined as a plasma sodium level
below135mmol/L, but symptoms such as lethargy, restlessness,and
disorientation generally only occur once plasma levelsdrop to
115–120mmol/L. Symptoms of hyponatraemia rarelyoccur unless
patients continue to drink excessive amountsof water (>10
litres/day) after maximum urine dilution isreached (100mOsm/kg
withminimumurine osmolality) andthe antidiuretic hormone of the
patients is fully suppressed[1]. When the kidney’s capacity to
compensate for exag-gerated water intake is exceeded, hypotonic
hyperhydrationresults.The consequences can involve headaches,
behaviouralchanges, muscular weakness, twitching, vomiting,
confusion,irritability, drowsiness, and seizures. Cerebral oedema
can
lead to brain damage and eventual death [2]. As in the
caseoutlined above, tonic-clonic seizures are the most
commonlyidentified presenting symptom, occurring in up to 80%
ofinitial presentations [3].
Differential diagnoses for hyponatraemia include SIADH,diabetes
insipidus, hyperthyroidism, and excess cortisol.Extreme water
consumption, as in the case outlined, is alsoimplicated [4].
Psychogenic polydipsia is a disorder that canlead to significant
morbidity and mortality and occurs in 6%to 20% of psychiatric
patients [1, 5]. Although psychogenicpolydipsia is relatively
common in this population, onlyone-fifth to one-third of polydipsic
patients will experiencesymptomatic hyponatraemia [6]. A number of
psychiatricdisorders have been linked with psychogenic polydipsia.
Themost commonly reported psychiatric disorder is
chronicschizophrenia, but it may also occur in anorexia nervosa[2]
and psychotic depression and bipolar psychosis [7, 8]. Aspecific
link to previous alcohol misuse has been found [9], adiagnosis
which, along with bipolar disorder with psychoticsymptoms, applies
to the patient described in this report.Thelatter study found rates
of alcohol abuse over three timesgreater in schizophrenic patients
with polydipsia than inthose without.
The aetiology of psychogenic polydipsia is uncertain andis
likelymultifactorial [1]. Impairedwater excretion
andwaterintoxication were noted in the psychiatric literature of
theearly 20th century, prior to the introduction of
antipsychoticmedication. The antidiuretic hormone, arginine
vasopressin(AVP), has been implicated. In normal circumstances,
thebrain carefully regulates the concentration of solute in
tissues,maintaining it within a very narrow range by controllingthe
secretion of AVP from the hypothalamus. Irrespective offluid
intake, this system can precisely regulate the internalmilieu.
Evidence suggests that the osmotic set point forAVP secretion may
be lower in patients with polydipsia andhyponatraemia, leading to
impairment in water excretion.Psychological stress and acute
psychosis may contribute tothis transient resetting of the osmostat
[10]. Other postulatedhypotheses include stimulation of thirst
centres by elevateddopamine levels, drinking to counteract
anticholinergic sideeffects of psychotropic medications, and
changes in feedbackregulation of the hypothalamic-pituitary axis
induced bychronic polydipsia [1].
Antipsychotics have been recognised to lower the
seizurethreshold [11], including olanzapine, which was prescribedto
the patient in this study [12]. This may have played apart in the
above case. The patient had had ECT threemonths prior to the
admission, but a literature search failedto indicate any link
between ECT and hyponatraemia. NoEEG had been carried out at
baseline. Sodium valproate, withits antiepileptic properties, had
been stopped the day beforethe seizure occurred. Also interesting
is the observation thathyponatraemia can worsen psychotic symptoms
and earlysigns of sodium deficiencymaymimic psychosis [13] or
bipo-lar disorder [14]. This has been more commonly recognisedin
the elderly butmay apply to the patient described,
whowassufficiently well once his hyponatraemia was corrected to
betreated, albeit intensively, in the community.
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Case Reports in Psychiatry 3
This case highlights the potentially catastrophic effectsof
psychogenic polydipsia. The phenomenon is not a newone, but this
case highlights a slightly different viewpointwhich is thatwhether
hyponatraemia is an independent resultof psychogenic polydipsia, or
whether indeed it, in itself,introduces a vicious circle, leading
to hyponatraemia thatcausesmany of the psychiatric sequelae. In the
case described,the patient’s behaviour significantly deteriorated
between thedate of his normal CT scan and the day of his seizure.
Thedeterioration was attributed purely to his psychosis, but
weargue that consideration must be given to the possibility, insuch
patients, that the symptoms are generated by a physicalcause,
hyponatraemia in this case, rather than assuming thatthe original
psychiatric illness is to blame.
Given how common psychogenic polydipsia is, we sug-gest that
routine enquiry should bemade into excessive waterintake, in both
inpatient and outpatient settings. Nursingstaff, who observe
patients continuously on a ward, should beeducated about the
importance of detection andmanagementof the condition. Bear in mind
that the differential diagnosisof symptoms of polyuria and
polydipsia includes diabetesinsipidus and mellitus, Addisonian
crisis, Conn’s syndrome,and chronic renal failure [2]. In general,
sodium levelsbetween 130 and 135mmol/L are asymptomatic,
anddecisionsregarding referral or assessment by a medical team
shouldbe based on the patient’s overall condition. Hospital
admis-sion is generally necessary for many patients with
sodiumlevels below 130mmol/L and for almost all with sodiumless
than 125mmol/L. Neurological signs in conjunctionwith hyponatraemia
always necessitate referral [15]. Cautionmust be taken in
correction of hyponatraemia as centralpontine myelinolysis may
occur if correction is overly rapid.Guidelines suggest a correction
rate of less than 10mmol/Lover the course of 24 hours [16]. In
terms of management ofpersistent psychogenic polydipsia,
therapeutic options suchas strict fluid restriction and behavioural
approaches havebeen found to be effective in reducing its severity
[17].
Conflict of Interests
The authors declare that there is no conflict of
interestsregarding the publication of this paper.
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